血小板活化以粘合剂配体和兴奋性血小板激动剂(在血管创伤位点释放或产生)的初始结合开始于血小板膜上的同源受体(Ruggeri 2002)。然后细胞内信号传导反应增强旋转血小板或血小板的粘合剂和血小板在接近循环的血小板。一旦血小板粘附脱滴,释放,释放储存的次级剂,如ADP,ATP和合成血栓素A2。这些扩增响应,激活和募集进一步的血小板和促进血小板聚集。这些扩增响应,激活和募集进一步的血小板和促进血小板聚集。腺苷核苷酸信号通过血小板膜上的P2嘌呤能受体。ADP激活P2Y1和P2Y12,其通过α和γ:β组分的信号(Hirsch等人,2001,2006),而ATP激活离子孔P2X1受体(Kunapuli等,2003)。这些受体的激活引发了复杂的信号级联,最终导致血小板活化,聚集和血栓形成(Kahner等人2006)。整合素Alphaiibbeta3是最丰富的血小板受体,每个休息血小板40 000至80000份拷贝,作为纤维蛋白原和其他粘合剂分子的主要受体(Wagner等,1996)。Alphaiibbeta3的激活增强了粘附性并导致血小板血小板相互作用,从而产生聚集(Philips等,1991)。 GP VI is the most potent collagen receptor initiating signal generation, an ability derived from its interaction with the FcRI gamma chain. This results in the phosphorylation of the gamma-chain by non-receptor tyrosine kinases of the Src family (1). The phosphotyrosine motif is recognized by the SH2 domains of Syk, a tyrosine kinase. This association activates the Syk enzyme, leading to activation (by tyrosine phosphorylation) of PLC gamma2 (2). Thrombin is an important platelet agonist generated on the membrane of stimulated platelets. Thrombin acts via cell surface Protease Activated Receptors (PARs). PARs are G-protein coupled receptors activated by a proteolytic cleavage in an extracellular loop (Vu, 1991) (3). Activated PARs signal via G alpha q (4) and via the beta:gamma component of the G-protein (5). Both stimulate PLC giving rise to PIP2 hydrolysis and consequent activation of PI3K (6). PLCgamma2 activation also gives rise to IP3 (7) which stimulates the IP3 receptor (8) leading to increased intracellular calcium. Platelet activation further results in the scramblase-mediated transport of negatively-charged phospholipids to the platelet surface. These phospholipids provide a catalytic surface (with the charge provided by phosphatidylserine and phosphatidylethanolamine) for the tenase complex (formed by the activated forms of the blood coagulation factors factor VIII and factor I).